Direct quotes from the article are in bold and italicized. My commentary follows each quote.

“The loss in mtDNA was associated with a delayed loss in mitochondrial function. Here, we report that the 4-quinolone drug ciprofloxacin is cytotoxic to a variety of cultured mammalian cell lines at concentrations that deplete cells of mtDNA.”

Ciprofloxacin depletes mitochondrial DNA in mammalian cells. It’s right there in black and white. I have no idea why it didn’t strike anyone as alarming when it was published in 1996. It sure is alarming now.

It should be noted that, “There is indeed experimental evidence that prolonged injury to mitochondria, such as that which typifies oxidative injury to mitochondrial DNA or to components of the electron transport chain (ETC), has to cross a certain threshold (or a number of thresholds) before cell damage or cell death becomes manifest.” (source) And that mitochondrial damage is linked to “symptoms such as fatigue, muscle pain, shortness of breath, and abdominal pain can easily be mistaken for collagen vascular disease, chronic fatigue syndrome, fibromyalgia, or psychosomatic illness.” (source) Mitochondrial dysfunction has been linked to multiple diseases of modernity including autoimmune diseases, neurodegenerative diseases, autism and “mysterious” diseases such as fibromyalgia and ME/CFS.

Also, as I’ve pointed out before, the FDA has noted in their internal documents that fluoroquinolones are toxic to mitochondria, and that mitochondrial damage is linked to many diseases, including neurodegenerative diseases. More information about that can be found in the post, “FLUOROQUINOLONE ANTIBIOTICS DAMAGE MITOCHONDRIA – FDA DOES LITTLE”

“Resistance was not due to a decrease in cellular drug accumulation, suggesting that ciprofloxacin cytotoxicity is caused by the loss of mtDNA-encoded functions. Analysis of mtDNA from ciprofloxacin-treated cells revealed the presence of site-specific, double-stranded DNA breaks.”

Consequences? Implications? What happens when cytotoxicity is induced by DNA breaks?

“These results suggest that ciprofloxacin may be causing cytotoxicity by interfering with a mitochondrial topoisomerase Il-like activity, resulting in a loss of mtDNA.”

Many assert that fluoroquinolones only affect bacterial topoisomerases. It turns out that mitochondrial topoisomerases are affected too. Fluoroquinolones should be used as prudently and cautiously as all other topoisomerase interrupting drugs. All the other topoisomerase interrupting drugs are chemo drugs that are only used to treat cancers. To prescribe a drug that depletes mitochondrial DNA and affects human topoisomerases in order to treat urinary tract infections and traveler’s diarrhea is absurd, short-sighted and wrong.

It should also be noted that, “Our data suggest that chemicals or genetic mutations that impair topoisomerases, and possibly other components of the transcription elongation machinery that interface with topoisomerases, have the potential to profoundly affect expression of long ASD (autism spectrum disorder) candidate genes. Length-dependent impairment of gene transcription, particularly in neurons and during critical periods of brain development, may thus represent a unifying cause of pathology in many individuals with ASD and other neurodevelopmental disorders.” (source)

The team of scientists who wrote that last quote are looking at whether or not fluoroquinolones turn on genes that are related to autism. The results of their exploration have not yet been published.

What is known though, is that topoisomerases are really important. Duh–they’re the enzymes responsible for proper DNA and RNA replication—did someone think they were optional? Interrupting topoisomerases with drugs is a really, really, really bad idea.

“Studies have also suggested that 4-quinolones may interfere with cell growth by inhibiting mammalian mtDNA replication (6, 11). Castora et al. (11) found that the 4-quinolone drugs nalidixic acid and oxolinic acid inhibited mtDNA replication in isolated rat liver mitochondria. These investigators inferred that this effect might be mediated by the inhibition of a mitochondrial topoisomerase II activity related to the bacterial enzyme DNA gyrase.”

Naladixic acid is the backbone of all fluoroquinolone antibiotics. The quote speaks for itself.

“We recently demonstrated that the 4-quinolone drugs nalidixic acid and ciprofloxacin cause a selective loss of mtDNA in drug-treated mammalian cells (6). The loss of mtDNA was associated with a decrease in mitochondrial respiration and an arrest in cell growth. These results suggested that inhibition of mammalian cell proliferation by 4-quinolone drugs might be caused by the selective depletion of mtDNA, resulting in compromised mitochondrial activity. We now report that ciprofloxacin causes a delayed cytotoxicity in cultured mammalian cells at concentrations that deplete cells of mtDNA.”

DELAYED CYTOTOXICITY! When someone says that you “shouldn’t” be experiencing an adverse reaction to a fluoroquinolone weeks, months or even years after you took the drug, show them this. Delayed cytotoxicity and mtDNA depletion–they’re right there. Fluoroquinolones are NASTY drugs. Why they are used frivolously is beyond my comprehension.

“We previously demonstrated that ciprofloxacin induces a selective depletion of mtDNA in mammalian cells. The depletion of mtDNA preceded a decrease in mitochondrial respiration and cell growth, suggesting that mtDNA was a primary target of drug action (6). Studies have recently shown that some cultured mammalian and avian cells can survive in the absence of mtDNA-encoded functions if the growth medium is supplemented with pyrimidines, pyruvate, and elevated concentrations of glucose (21-23). Cells deficient in mtDNA rely exclusively on glycolysis for energy.”

Hmmmmm…. So do our cells need/want more glucose??

And, again, I’d like to point out the clearly stated, “ciprofloxacin induces a selective depletion of mtDNA in mammalian cells.”

“The apparent decrease in mtDNA cleavage at higher drug concentrations is reminiscent of the effect of DNA intercalating anticancer drugs on nuclear topoisomerase II enzymes (29, 30). Intercalating anticancer drugs such as 2-methyl-9-hydroxyellipticinium and Adriamycin have been shown to stimulate topoisomerase II cleavage at low concentrations but inhibit cleavage at high drug concentrations.”

“The non-exonuclease-treated DNA contained both linear and nicked circular forms of mtDNA but did not contain closed circular supercoiled mtDNA (Fig. 8, lane A), suggesting that ciprofloxacin induces single- as well as double stranded protein-linked breaks in the mtDNA.”

Thanks for breaking my DNA, Bayer.

“The current results indicate that ciprofloxacin is not cytotoxic unless cells are continuously exposed to drug for a minimum of three or four cell doublings. In comparison, drugs that target nuclear topoisomerase II trigger an apoptotic type of cell killing, even after a short 2-hr drug exposure.”

Interesting. What is the time-frame for cell doubling? And I don’t think that the question has been definitively answered as to whether or not fluoroquinolones are stored in lipids, continuously exposing cells to damage, or not.

“Another possibility is that the growth inhibitory and cytotoxic effects of ciprofloxacin are caused by the inhibition of an essential mitochondrial function or functions. This is supported by the following observations: First, treatment of mammalian cells with ciprofloxacin results in a selective depletion of mtDNA, leading to a decrease in mitochondrial respiration (6). These mitochondrial events precede the drug induced loss in cell growth and viability (Ref. 6 and current results). Second, cells become resistant to ciprofloxacin when they are grown under conditions that do not require mtDNA encoded functions. Third, ciprofloxacin induces the formation of site-specific, protein-linked breaks in mtDNA, indicating the presence of a drug-sensitive mitochondrial topoisomerase Il-like activity.”

Given the connections between ciprofloxacin and mitochondrial damage–depleting mtDNA and decreasing mitochondrial respiration, and the connections between mitochondrial damage and multiple chronic, multi-symptom illnesses, it is not absurd to make the assertion that ciprofloxacin, and other fluoroquinolones, can cause those diseases (autoimmune diseases, neurodegenerative diseases, fibromyaligia, autism, ME/Chronic Fatigue Syndrome, etc.).

It’s nice and dandy that “cells become resistant to ciprofloxacin when they are grown under conditions that do not require mtDNA encoded functions” but human beings don’t have a bunch of cells that live in petri dishes that can grow without requiring our mitochondrial DNA functions. I wonder what happens when human cells attempt to adapt to resist ciprofloxacin and adapt by ceasing to require mtDNA encoded functions. I bet you a buck that no one knows the answer to that question.

Cipro breaks mitochondrial DNA. WHY WASN’T THIS REPORT PAID ATTENTION TO? All of the results in it warrant fluoroquinolones being taken off of the market until further investigation can be done. This is absurd. I know that there are cases where fluoroquinolones can save lives, I get that, and I’m usually decently reasonable about not calling for their removal from the market. But this article spooked me severely. We, collectively, have NO CLUE what the consequences of depleting our mitochondrial DNA are.

“Neither cell growth nor viability seems to be affected until cells have undergone three or four cell doublings in the presence of ciprofloxacin (Ref. 6 and current results). During this time span, the content of mtDNA decreases >90%, suggesting that drug is causing a loss in cell growth and viability by interfering with mtDNA replication.”

Nasty drugs – but if you metabolize them fast enough, they’re less nasty – apparently.

“Ciprofloxacin, as well as several other 4-quinolone drugs, can cause significant unwinding of DNA”

It’s what they’re designed to do. They’re topoisomerase interrupters. The mechanism of action for ciprofloxacin is, “The bactericidal action of ciprofloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV (both Type II topoisomerases), which are required for bacterial DNA replication, transcription, repair, and recombination.” (source) It doesn’t take a rocket scientist to realize that drugs that inhibit the DNA and RNA replication, transcription, repair and recombination are dangerous. I hate the FDA for allowing these dangerous drugs to be used as antibiotics. It’s ludicrous.

“Delayed Cytotoxicity and Cleavage of Mitochondrial DNA in Ciprofloxacin-Treated Mammalian Cells” is not a hopeful article. It is, frankly, a terrifying article. More than 20 million prescriptions for fluoroquinolones are given out in Americans each year for the last couple decades, and that’s only a small portion of the prescriptions given worldwide. What have we done to our collective mitochondrial DNA?? What are the consequences of depleting our mitochondrial DNA? No one knows the answers to those questions.

Anyone who thinks that people aren’t sick with the diseases related to mitochondrial poisoning, isn’t looking very hard. People are sick. They’re in pain (peripheral neuropathy is thought to be caused by mitochondrial malfunctions), they’re depressed and suffering from even worse psychiatric disorders, they have heart conditions and metabolic disorders (source), ME/Chronic Fatigue Syndrome, autism, and many other misunderstood, chronic illnesses. There are many potential culprits for the sorry state of human health in the 21st century, but fluoroquinolones aren’t even on the list according to most people.

FLUOROQUINOLONES DEPLETE MITOCHONDRIAL DNA, LEAD TO MITOCHONDRIAL DYSFUNCTION AND ALSO OBLITERATE THE MICROBIOME!

I’ll keep screaming it until I’m heard.

Back in 1992 it was noted that, “the interaction (of fluoroquinolones) with DNA is still of great concern because of the possible long-term genotoxicity of quinolone compounds, which are increasingly adopted as first-choice antibiotics for the treatment of many infections, and because it addresses the real mechanism of action of this class of molecules.” (source)

I really wish that these warnings had been heeded. Sadly, they’ve been ignored.

Our poor mitochondrial DNA. I hope that mtDNA recovers and that the situation isn’t as dire as I suspect. But the truth is, no one knows. No one has a clue what the consequences of depleting mtDNA through unnecessary use of topoisomerase interrupting drugs are.

Floxies certainly know that the consequences of fluoroquinolones can involve a massive amount of pain and suffering. It’s not okay.

Bayer, Johnson & Johnson, the FDA and everyone else involved with frivolously prescribing these drugs should be ashamed of themselves for failing to protect our mitochondrial DNA. Topoisomerase interrupters should never have been approved for use as antibiotics. It’s simply absurd.

I recently read “Cooked: A Natural History of Transformation” by Michael Pollan. You can buy it HERE and a portion of the proceeds will go to the QVF. I recommend that you purchase it, not just because some money will go to the QVF, but because it is beautifully written, enjoyable, interesting, insightful and poignant.

On the surface, Cooked has very little, if anything, to do with fluoroquinolone antibiotic toxicity. Cooked is about the transformation of raw ingredients into food when fire, water, air and earth are applied to those ingredients through the process we call cooking. The section of Cooked that has to do with how things from the earth–bacteria, fungi, etc., are used to transform and “cook” food, is the section I am going to connect to fluoroquinolone antibiotic toxicity.

Fluoroquinolone antibiotics are like a nuclear bomb to the gut. They obliterate the microbiome, killing both good and bad bacteria in the gut and throughout the body. They lead to a massive amount of oxidative stress within the gut that further damages the balance of bacteria in the gut. It is only because of lack of knowledge about the importance of the microbiome that Cipro/ciprofloxacin only has a 43 page warning label, not a 100 page warning label. In Cooked, Michael Pollan goes over the importance of the microbiome. He explains the microbiome better than I possibly could, so I’m going to highlight some of my favorite quotes from Cooked in this post.

“Could it be possible that the microbiota also affects mental function and mood, as some of the fermentos I met in Freesone claimed? The idea no longer seems preposterous. A recent study performed in Ireland found that introducing a certain probiotic species found in some fermented foods (Lactobacillus rhamnosus JB-1) to the diet of mice had a measureable effect on their stress levels and mood, altering the levels of certain neurotransmitters in the brain. Precisely how the presence of a certain bacterium in the gut might affect mental function is unclear, yet the researchers found they could block the effect by severing the vagus nerve that links the gut to the brain. Studies like this one make you wonder if it might someday be possible to cultivate, or garden, our microbiota, altering its makeup to improve our physical and possibly also our mental well-being.

Right now, of course, and for the last several decades at least, we have been assiduously doing exactly the opposite: disordering the community of microbes in our bodies without even realizing it, much less with any sense of what might be at stake. Under the pressures of broad-spectrum antibiotics, a Pasteurian regime of ‘good sanitation,’ and a modern diet notably hostile to bacteria, the human microbiota has probably changed more in the last hundred years than in the previous ten thousand, when the shift to agriculture altered our diet and lifestyle. We are only just beginning to recognize the implications of these changes for our health.”

“The average child in the developed world has also received between ten and twenty courses of antibiotics before his or her eighteenth birthday, an assault on the microflora the implications of which researchers are just beginning to reckon. Like the pesticides applied to a farm field, antibiotics ‘work,’ at least in the short term. Yet as soon as you widen the lens from a narrow focus on the ‘enemy species,’ you see that such blunt weapons inflict collateral damage to the larger environment, including, in the case of pesticides, the microbial community of the soil. Resistant bugs and various other health problems soon emerge; the soil’s ability to nourish plants and help them withstand disease is also compromised, because the toxins have reduced the community’s biodiversity and thereby compromised its resilience. As in the soil, so in the gut. The drive for control and order ends up leading to more disorder.”

“An interesting question is why the body would enlist bacteria in all these critical functions, rather than evolve its own systems to do this work. One theory is that, because microbes can evolve so much more rapidly than the ‘higher animals,’ they can respond with much greater speed and agility to changes in the environment–to threats as well as opportunities. Exquisitely reactive and fungible, bacteria can swap genes and pieces of DNA among themselves, picking them up and dropping them almost as if they were tools. This capability is especially handy when a new toxin or food source appears in the environment. The microbiota can swiftly find precisely the right gene needed to fight it–or eat it.”

“Taken together, the microflora may function as a kind of sensory organ, bringing the body the latest information from the environment, as well as the new tools needed to deal with it. ‘The bacteria in your gut are continually reading the environment and responding,’ says Joel Kimmons, a nutrition scientist and epidemiologist at the Centers for Disease Control and Prevention in Atlanta. ‘They’re a molecular mirror of the changing world. And because they can evolve so quickly, they help our bodies respond to changes in our environment.”

Another book of Michael Pollan’s, “The Omnivore’s Dilemma: A Natural History of Four Meals” goes over the hazards of applying the industrial model to biological systems–specifically, the folly of using the industrial model to produce food when food production should be a biological, not an industrial, process. The same is true for medicine. The medical system treats people as machines with inputs and outputs and predictable outcomes based on those measured inputs and outputs. It doesn’t work though. Humans are biological systems with feedback and feedforward loops, genetic differences and epigenetic differences, nature and nurture differences, and more–that make conceptualizing humans as machines with predictable outcomes foolish and wrong-headed. When land and animals are used to make food in an industrial, rather than biological, model, unsustainability, externalities and consequences result. When biological systems are respected for the complex systems that they are, sustainability comes naturally. Likewise, when human complexity is ignored and stupid, foolish, one-size-fits-all, industrial medicine prevails, consequences occur in place of health. It turns out that consequences look a whole lot like chronic illness. Whoops.

Lisa’s one-sentence summary of Cooked and The Omnivore’s Dilemma is – Don’t eat processed food. Read the books for a more thorough explanation. They’re both excellent.

In Episode 10 of The Floxie Hope Podcast Ariel shares her journey through fluoroquinolone toxicity. Ariel felt and looked like she had aged 15 years in a matter of just a couple months after she took ciprofloxacin to treat a urinary tract infection. She also suffered from anxiety, insomnia, depersonalization and many areas of her life falling apart. Though Ariel is still going through her fluoroquinolone toxicity journey, she has learned many life lessons along the way. She has found her strength and joy has returned to her life. Ariel brings beautiful perspective to the journey through fluoroquinolone toxicity.

The Wahls Protocol frightens me because of how similar multiple sclerosis (MS) is to fluoroquinolone toxicity. Dr. Wahls goes over how mitochondrial damage is linked to autoimmune diseases, especially MS. Fluoroquinolones profoundly damage mitochondria. Fluoroquinolone toxicity looks and feels a whole lot like multiple autoimmune diseases including rheumatoid arthritis, lupus and MS. Some people have proposed that fluoroquinolone toxicity is its own autoimmune disease, just the auto-antibodies have not yet been identified and thus it is not treated as an independent autoimmune disease. In some people, fluoroquinolones have triggered a recognized autoimmune disease, as you can read about in Michelle’s Story of fluoroquinolone induced lupus, and I have another friend with fluoroquinolone induced MS.

There is nothing more frightening to me than an autoimmune disease. Having my body attack itself sounds absolutely horrible. I hate the thought. I turn off, get nauseous, and resist every time I hear the suggestion that fluoroquinolone toxicity is an autoimmune disease.

MS causes brain lesions, weakness and paralysis, and typically requires drug treatments that are almost as horrible as the disease itself. MS is terrifying. I HATE the thought that fluoroquinolone toxicity might be unrecognized MS with different antibodies.

I tell myself, “I don’t have MS, I got poisoned. I know my poison – Cipro. It kicked me but I got back up. My body isn’t attacking itself for no reason. I got poisoned.” It makes me feel a little bit better.

Even though The Wahls Protocol is a hopeful book, with lots of lifestyle change suggestions that have reversed the course of autoimmune diseases in many people, and the diet and suggestions that Dr. Wahls makes will almost certainly help floxies (including me), I’m still struggling with it. It’s really difficult for me to face the notion that my reaction to Cipro may have been an autoimmune reaction. I don’t like that thought at all.

I realize that it may seem otherwise, but I really don’t like being able to connect fluoroquinolone toxicity to autoimmune or neurodegenerative diseases. Unfortunately, mitochondrial damage and oxidative stress are hallmarks of both.

As I read The Wahls Protocol, I wonder if I got hit with fluoroquinolone toxicity because I have a genetic predisposition toward malfunctioning cells. Maybe my cells don’t detoxify xenobiotics as well as the cells of other people. Perhaps the mechanisms that protect my mitochondria aren’t as robust as they need to be to survive in this environment, and my cells are likely to react in a way that involves making me sick when I am exposed to pharmaceutical and environmental poisons in the future.

I hate that thought. It makes me feel weak and as if there is something wrong with me.

I tell people all the time, “You’re sick, you’re not broken, and you’ll get better.” I mean it. I believe it’s true.

I got better. I recovered from fluoroquinolone toxicity. But I wonder if my cells are a bit broken, or at least breakable.

I don’t like acknowledging my weaknesses any more than anyone else. I hate it.

But in acknowledging that I am susceptible to getting poisoned, maybe I can gain power. Maybe that knowledge can save me hardship and suffering down the road. Maybe that knowledge can help me to avoid mitochondrial poisons in the future.

Guidelines and methods for how to both avoid future damage and how to put my cells back together are available in The Wahls Protocol. If I can calm my nerves enough to get through it, I’m sure I’ll gain a lot from the book.

Renee recovered from fluoroquinolone toxicity through using the methods described in The Wahls Protocol. Dr. Wahls’ TED talk (below) about her journey through MS and recovery is both beautiful and inspirational. There is a road to recovery from autoimmune diseases. Maybe I shouldn’t feel so scared of them.

In Episode 9 of The Floxie Hope Podcast I had the opportunity to interview Rick Radcliff. Rick is a long-time flox survivor. He was hurt by Avelox/moxifloxacin ten years ago.

In the ten years that Rick has been a floxie, he has learned a lot about fluoroquinolone toxicity. He reveals a lot of interesting information about the links between fluoroquinolone induced mitochondrial damage and thyroid health. Balancing his hormones has helped him to improve immensely.

Please listen to Rick’s story and share it with your friends. Thank you!

In 1992 the fluoroquinolone antibiotic Omniflox/temifloxacin was removed from the US market after causing three deaths.

To note the removal from the market, the FDA released the following statement:

“The Food and Drug Administration today announced that Abbott Laboratories of Abbott Park, Ill., is voluntarily recalling the broad-spectrum anti-infective drug Omniflox (temafloxacin) tablets, and will halt all further distribution of the drug.

This action is being taken because of severe adverse events associated with the use of the drug that have been reported to the company and to FDA in the first three months of marketing.

Temafloxacin was approved in late January 1992 and marketed in mid-February. Since that time there have been approximately 50 reports of serious adverse reactions, including three deaths. There were several cases of severe low blood sugar, especially in very elderly patients with decreased kidney function. Among the severe reactions there were a number of cases of an unusual complex of adverse reactions consisting of hemolitic anemia (destruction of red blood cells) and other blood cell abnormalities.”

I’m glad that Omniflox/temafloxacin was removed from the market. I’m glad that, in 1992, the FDA was able to move quickly to do the right thing and take a dangerous drug off the market.

It begs the question though – Why is Levaquin/levofloxacin still on the market?

Assuming that only 10% of the harm was reported, 9,240 people (including 30 children) were killed by Levaquin/levofloxacin in the 12 years measured.

Additionally, there were 10,166 reports of harm done by Levaquin/levofloxacin in that time period. If that’s 10% of the actual harm done, 101,660 people were harmed by Levaquin/levofloxacin in that 12 year period.

Again, THREE people died from Omniflox/temafloxacin before it was promptly pulled from the market in 1992. Johnson & Johnson is apparently on friendlier terms with the FDA than Abbott Labs.

Rest in Peace Chris Dannelly

Since 2008, Levaquin/levofloxacin has claimed many more victims. Chris Dannelly is one of the people who tragically died after taking levofloxacin in January, 2013. Chris was a 41 year old husband and father of two young kids. He was an athlete at the prime of his life.

Chris was killed by two pills of levofloxacin. You can read Chris’s story HERE. From Chris’s Story, “After reviewing the autopsy report, doctors stated that ‘all signs point to Levaquin’ as being the cause of death.” And, “Chris was a healthy, active man in the prime of his life. He worked out five days per week, and enjoyed playing both indoor and outdoor soccer regularly. Within a matter of less than a week’s time he went from being perfectly healthy, to losing his life…all because he took two little pills of Levaquin.”

Chris’s tragic story, highlighted by WSB-TV 2 out of Atlanta, Georgia, and told by Chris’s brave wife Kathy, can be viewed here –

Kathy states in the interview, “If I can get involved in this drug somehow coming off the market one day – then that’s the least I can do.”

Also on WSB-TV 2 Atlanta, Sandy Davis tells the story of how her husband Richard was killed by Levquin/levofloxacin:

Sandy Davis states, “I don’t think it should even be on the market. If it’s killing people – No.” Indeed. Richard was 60 years old when he passed.

But, but, but…

People will argue that we need Levaquin/levofloxacin because bacterial resistance to antibiotics is making more powerful antibiotics necessary. There may be some truth to that argument. But rather than seeing dangerous, complex drugs like Levaquin/levofloxacin in simplistic black and white terms, perhaps some thoughtful consideration of the grey area is in order.

IF it is deemed impossible for the FDA to remove Levaquin/levofloxacin from the market (and I do believe that it should be taken off the market – it is, after all, KILLING PEOPLE), it should be severely restricted. Levaquin/levofloxacin should ONLY be used in life or death situations. It should ONLY be used when all other non-fluoroquinolone antibiotic options have been exhausted. It should ONLY be used in patients who haven’t previously been exposed to fluoroquinolones. It should ONLY be used in people who are not genetically predisposed toward an adverse reaction to fluoroquinolones. (Who is genetically predisposed toward an adverse reaction to Levaquin/levofloxacin? Good question. Figure it out, FDA.) It should NEVER be given to children, athletes, the elderly, those with an autoimmune disease, those with autonomic nervous system dysfunction, those with a history of psychiatric illness, or anyone who needs to use contraindicated drugs, like steroids and NSAIDs, to survive.

IF Levaquin/levofloxacin must stay on the market, everyone who takes it should be provided with information that ensures that they know that Levaquin/levofloxacin can cripple or kill them.

Before anyone insists that Levaquin/levofloxacin must stay on the market, perhaps we (collectively) should do some due diligence to make sure that it, and other fluoroquinolone antibiotics, don’t have intergenerational adverse effects. After all, their mechanism of action is interruption of topoisomerase enzymes, enzymes that are necessary for DNA and RNA replication. In case it needs to be said, disrupting the DNA and RNA replication process of cells may have some deleterious effects on future generations. Don’t assume for a second that this concern has been examined. Warnings about the DNA toxicity of fluoroquinolone antibiotics have been ignored.

Though I understand that antibiotic resistance and loss of antibiotic efficacy is a problem, I can’t say that I entirely buy arguments that Levaquin/levofloxacin must stay on the market. No one claims that we are worse off because Omniflox/temafloxacin was removed from the market. Infections were also being adequately treated by non-fluoroquinolone antibiotics prior to 1987, when Levaquin/levofloxacin was approved by the FDA.

Kathy Dannelly and her children, Sandy Davis and her loved ones, and all other loved ones of victims of Levaquin/levofloxacin deserve justice. Many of them aren’t getting justice. The least that the FDA can do is keep others from dying in pain from fluoroquinolone toxicity caused by Levaquin/levofloxacin.